Gut Feeling
By Nathan Seppa
May 28th, 2008
sciencenews.org
Probiotic microbe kicks on an anti-inflammatory process in mice
We are all crawling with bacteria, and researchers hope someday to
induce some of these microbes within us to produce compounds that will
fight disease. In a first step toward this goal, a team has identified
a bacterial product that kicks on anti-inflammatory machinery in the
intestines of mice and suppresses a condition similar to human Crohn’s
disease.
The findings offer the first example of a microbe-generated compound
that “networks” with the immune system to quell inflammation in a
mammal, the scientists report in the May 29 Nature.
The human intestines house 300 to 1,000 distinct kinds of bacteria —
some good and some bad. Many have never been clearly identified or
even accurately counted. Their roles are also gradually being
discerned to include more than food digestion.
But from an evolutionarily perspective, it’s a safe assumption that
humans would have purged these bacteria long ago if the microbes had
no purpose or were strictly detrimental, says Marika Kullberg, an
immunologist at the University of York in England.
Since incidence of inflammatory bowel ailments such as Crohn’s disease
have risen sharply in the West since the 1950s, identifying which gut
bacteria have anti-inflammatory roles could be a boon to medicine.
With that in mind, physician and microbiologist Dennis Kasper of
Harvard Medical School in Boston and his colleagues tested mice that
were bred to lack intestinal microbes. Using this living blank slate,
the researchers induced inflammation in the animals’ colons and
simultaneously fed the mice a microbe called Bacteroides fragilis.
Earlier work had suggested that this bug has anti-inflammatory
properties.
Introducing B. fragilis prevented inflammation. Further tests reveled
that the bacterium produces a sugar called polysaccharide A, which
induces immune cells to crank out an anti-inflammatory protein called
interleukin-10. Feeding the sugar directly to the mice also inhibited
inflammation in the animals, the researchers report.
Whether these results will translate to people is another matter,
Kasper says, since interleukin-10 has a short half-life in people.
Nevertheless, studies like this “are pieces of the puzzle,” says
Kullberg, who wasn’t involved in the research. “With more pieces, you
get a better overview of how the system works.”
Inflammatory bowel diseases might result from an inappropriate immune
attack on microbes — good and bad — in the gut, says Kullberg.
Improved sanitation, a lifetime of antibiotic use and even vaccines
against bacteria may disrupt the microbial equilibrium people have
evolved to harbor in the gut, she says. In essence, some beneficial
microbes may die from friendly fire.
How this disruption might translate into chronic inflammation remains
unclear, she says. The cause of Crohn’s disease and other inflammatory
bowel disorders probably includes genetic predisposition and maybe
other factors, she says.
To sort out the mysteries of these gut flora, the National Institutes
of Health is sponsoring the Human Microbiome Project, which seeks to
identify the microbes that live within people and those microbes’
uses.
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